光动力疗法
肿瘤微环境
癌症研究
免疫疗法
免疫系统
癌症
癌症免疫疗法
医学
活性氧
癌细胞
免疫原性细胞死亡
免疫学
化学
内科学
生物化学
有机化学
作者
Xudong Zhu,Wenxuan Zheng,Xingzhou Wang,Zhiyan Li,Xiaofei Shen,Qi Chen,Yanjun Lu,Kai Chen,Shichao Ai,Yun Zhu,Wenxian Guan,Shankun Yao,Song Liu
标识
DOI:10.1002/advs.202307870
摘要
Abstract For tumor treatment, the ultimate goal in tumor therapy is to eliminate the primary tumor, manage potential metastases, and trigger an antitumor immune response, resulting in the complete clearance of all malignant cells. Tumor microenvironment (TME) refers to the local biological environment of solid tumors and has increasingly become an attractive target for cancer therapy. Neutrophils within TME of gastric cancer (GC) spontaneously undergo ferroptosis, and this process releases oxidized lipids that limit T cell activity. Enhanced photodynamic therapy (PDT) mediated by di‐iodinated IR780 (Icy7) significantly increases the production of reactive oxygen species (ROS). Meanwhile, neutrophil ferroptosis can be triggered by increased ROS generation in the TME. In this study, a liposome encapsulating both ferroptosis inhibitor Liproxstatin‐1 and modified photosensitizer Icy7, denoted LLI, significantly inhibits tumor growth of GC. LLI internalizes into MFC cells to generate ROS causing immunogenic cell death (ICD). Simultaneously, liposome‐deliver Liproxstatin‐1 effectively inhibits the ferroptosis of tumor neutrophils. LLI‐based immunogenic PDT and neutrophil‐targeting immunotherapy synergistically boost the anti‐PD‐1 treatment to elicit potent TME and systemic antitumor immune response with abscopal effects. In conclusion, LLI holds great potential for GC immunotherapy.
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